Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pseudomonas aeruginosa is the most prominent colonizer of the respiratory tract of patients with cystic fibrosis, but it is not known why this occurs. P. aeruginosa adheres to mucins from normal individuals, but mucins from cystic fibrosis patients have not been studied. To compare adhesion to mucins from cystic fibrosis with other mucins, we prepared highly glycosylated mucin glycopeptides from cystic fibrosis and chronic bronchitis patients by ion-exchange and gel-filtration chromatography and measured the adhesion of P. aeruginosa 1244 to these glycopeptides. We found (i) that the most mucinlike glycopeptides from P. aeruginosa-infected cystic fibrosis sputa showed less bacterial adhesion than did the corresponding bronchitis samples, (ii) that the most adhesive activity in cystic fibrosis samples came from a fraction that contains O and N glycopeptides and may be in part a degradation product of P. aeruginosa infection, and (iii) that highly glycosylated glycopeptides of the most acidic species (sialylated and sulfated) showed no adhesion at all. A single cystic fibrosis sample not infected by P. aeruginosa showed better binding in the adhesion-positive fractions than did the infected sputa. These studies suggest that cystic fibrosis mucins may be altered after infection is established, resulting in less binding to some fragments. However, since the clinical picture shows heavy mucus colonization, other receptors, such as cellular glycolipids which have been shed into mucus, may be contributing to this colonization.
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PMID:Differences in adhesion of Pseudomonas aeruginosa to mucin glycopeptides from sputa of patients with cystic fibrosis and chronic bronchitis. 277 73

Sputum from patients with chronic obstructive bronchitis has been fractionated on Sepharose columns after treatment with urea 6 mol/l at pH 12.5 followed by neutralization. The "mucin" fraction, which contained 70% carbohydrate and 30% protein was studied in the electron microscope after staining with phosphotungstic acid. Positively stained, thread-like, irregular contours of the mucin molecules could be demonstrated with lengths varying from 2,000 to 5,000 nm, corresponding to molecular weights between 2 X 10(6) and 6 X 10(6). This correlates fairly well with estimates from the literature of the size of these molecules.
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PMID:Electron microscopy of mucin from sputum in chronic obstructive bronchitis. 743 75

Airway mucus is a complex airway secretion whose primary function as part of the mucociliary transport mechanism is to to serve as renewable and transportable barrier against inhaled particulates and toxic agents. The rheologic properties necessary for this function are imparted by glycoproteins, or mucins. Some respiratory disease states, e.g., asthma, cystic fibrosis, and bronchitis, are characterized by quantitative and qualitative changes in mucus biosynthesis that contribute to pulmonary pathology. Similar alterations in various aspects of mucin biochemistry and biophysics, leading to mucus hypersecretion and altered mucus rheology, result from inhalation of certain air pollutants, such as ozone, sulfur dioxide, nitrogen dioxide, and cigarette smoke. The consequences of these pollutant-induced alterations in mucus biology are discussed in the context of pulmonary pathophysiology and toxicology.
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PMID:The role of airway mucus in pulmonary toxicology. 792 90

Bronchial casts are characterized by the formation of obstructive airway plugs that may be large enough to fill the branching pattern of an entire lung. The condition is rare but can occur at any age. Casts may be secondary to underlying diseases such as asthma and cystic fibrosis, but there are often no predisposing factors. There is no accepted classification system for bronchial casts; but only a confusion of descriptive terms such as mucoid impaction, fibrinous bronchitis, and pseudomembranous bronchitis. Based on a review of nine well-documented cases and the available literature, we have separated bronchial casts into two well-defined groups: Type 1 (inflammatory), consisting of casts composed mainly of fibrin with a dense eosinophilic inflammatory infiltrate; and Type 2 (acellular), consisting of casts composed mainly of mucin with little or no cellular infiltrate and occurring only in children with congenital cyanotic heart disease. Acute mortality was high in both groups. Survivors of Type 1 casts seem to be well controlled with inhaled steroids. Optimal therapy for patients with Type 2 casts is not clear; the prognosis probably depends on underlying cardiac status. We hope that this simple classification will provide a framework for further study of this obscure condition.
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PMID:Bronchial casts in children: a proposed classification based on nine cases and a review of the literature. 900 37

One hundred and forty five patients with different forms of dust-induced lung disease and 57 controls having no contacts with industrial aerosols were examined. It was ascertained that clinical and functional evidence cannot predict the course of the disease and the development of infectious complications (silicotuberculosis, mechanic bronchitis). Impaired humoral immunity and nonspecific resistance in dust-induced lung disease depend on the type of disease and predispose to infectious complications. Predisposition to occupational lung diseases (pneumoconioses, mechanical bronchitis) is associated with increases in the concentrations of plasma fibronectin and serum IgA and a decrease in serum mucin antigen levels. In chronic mechanical bronchitis, there were lower activities of lysozyme and complement and elevated serum IgM and IgG concentrations. Fibronectin, total IgE and the inflammatory marker the mucin antigen 3EG5 are involved in immunological inflammation in dust-induced lung disease. It is worth of determining the factors of humoral immunity and nonspecific resistance in workers contacting with high concentrations of industrial aerosols and in patients with dust-induced diseases to make a precise assessment of the time course of changes in a pathological process and to define a risk for infectious complications.
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PMID:[Immunological changes in dust-induced lung diseases]. 1131 68

Plastic bronchitis is characterized by marked obstruction of the large airways by bronchial casts. We reviewed our experience and the literature to determine whether mortality rates are determined by underlying disease or cast type. We present 3 children with obstructive bronchial casts. One 3-year-old patient with Noonan's syndrome developed respiratory failure following surgery for tetralogy of Fallot requiring support with extracorporeal membrane oxygenation (ECMO) the first such case. There were 42 cases in the literature of children with plastic bronchitis. Casts may be divided into two types. Type I casts are inflammatory, consisting mainly of fibrin with cellular infiltrates, and occur in inflammatory diseases of the lung. Type II, or acellular casts, consist mainly of mucin with a few cells, and usually occur following surgery for congenital cardiac defects. Patients categorized by underlying disease included 31% with asthma or allergic disease, 40% with underlying cardiac defects, and 29% with other diseases. Mortality was 16%, but increased to 29% in patients with cardiac defects. Deaths occurred as long as 1 year after surgical repair for underlying defects. There were no deaths in patients with asthma. Life-threatening events were statistically higher in patients with cardiac defects (41%) than in those with asthma (0%, P = 0.02). Higher mortality in patients with type II casts compared to type I casts did not reach statistical significance (28% vs. 6%; P = 0.06). In conclusion, patients presenting with plastic bronchitis are at high risk for serious complications, especially with underlying cardiac disease.
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PMID:Plastic bronchitis in children: a case series and review of the medical literature. 1242 47

Cystic fibrosis (CF) is characterized by progressive airway obstruction. Although it has been postulated that this is due in part to mucus hypersecretion, there are no published data showing an increase in the gel-forming mucins MUC5AC or MUC5B in CF secretions. We used confocal microscopy to assess the amount of mucin-like glycoprotein and DNA in CF sputum and found more mucin in bronchitis sputum and a much greater amount of DNA in CF sputum. We then used antibodies to MUC5AC and MUC5B with Western gels and dot-blot to quantify mucin in sputum from 12 patients with CF and 11 subjects without lung disease. There was a 70% decrease in MUC5B and a 93% decrease in MUC5AC in CF sputum (P < 0.005 for both). We conclude that the vol/vol concentration of MUC5AC and MUC5B are decreased in the CF airways relative to normal mucus. This may be due to a relative increase in other components of sputum in the CF airway or to a primary defect in mucin secretion in CF.
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PMID:MUC5AC and MUC5B Mucins Are Decreased in Cystic Fibrosis Airway Secretions. 1571 16

Chronic obstructive pulmonary disease (COPD) is characterized by airway obstruction, inflammation, and mucus hypersecretion, features that are common in bronchitis, emphysema, and often asthma. However, current rodent models do not reflect this human disease. Because genetically predisposed spontaneously hypertensive (SH) rats display phenotypes such as systemic inflammation, hypercoagulation, oxidative stress, and suppressed immune function that are also apparent in COPD patients, we hypothesized that SH rat may offer a better model of experimental bronchitis. We, therefore, exposed SH and commonly used Sprague Dawley (SD) rats (male, 13- to 15-weeks old) to 0, 250, or 350 ppm sulfur dioxide (SO(2)), 5 h/day for 4 consecutive days to induce airway injury. SO(2) caused dose-dependent changes in breathing parameters in both strains with SH rats being slightly more affected than SD rats. Increases in bronchoalveolar lavage fluid (BALF) total cells and neutrophilic inflammation were dose dependent and significantly greater in SH than in SD rats. The recovery was incomplete at 4 days following SO(2) exposure in SH rats. Pulmonary protein leakage was modest in either strain, but lactate dehydrogenase and N-acetyl glucosaminidase activity were increased in BALF of SH rats. Airway pathology and morphometric evaluation of mucin demonstrated significantly greater impact of SO(2) in SH than in SD rats. Baseline differences in lung gene expression pattern suggested marked immune dysregulation, oxidative stress, impairment of cell signaling, and fatty acid metabolism in SH rats. SO(2) effects on these genes were more pronounced in SH than in SD rats. Thus, SO(2) exposure in SH rats may yield a relevant experimental model of bronchitis.
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PMID:The spontaneously hypertensive rat: an experimental model of sulfur dioxide-induced airways disease. 1692 7

Plastic bronchitis is an uncommon condition characterized by the production of large pale bronchial casts that obstruct the tracheobronchial tree. The cellular content, cohesiveness, and often rubber-like consistency distinguish bronchial casts from the usual mucus plugs found with such disease states as asthma. Plastic bronchitis can be found secondary to many conditions, and a simplified classification scheme organizes it into two groups: an inflammatory type consisting of casts with an eosinophilic inflammatory infiltrate and an acellular type with a predominance of fibrin distinguished by its relative lack of cellular infiltrate, its mucin predominance, and its appearance only in children with congenital cyanotic heart disease. This report describes a 5-year-old girl who experienced plastic bronchitis 3 months after a Fontan procedure for hypoplastic left heart syndrome that was treated successfully with aerosolized tissue plasminogen activator.
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PMID:Fontan patient with plastic bronchitis treated successfully using aerosolized tissue plasminogen activator: a case report and review of the literature. 1900 18

The arylhydrocarbon receptor (AhR) is known for its ability to bind aromatic-containing compounds, which starts a molecular cascade involving the induction of cytochrome P450s and inflammatory cytokines. Our hypothesis is that many inhaled environmental toxicant components activate these inflammatory pathways via an initial binding to the AhR. To test this possibility, we treated Clara cell-derived NCI-H441 cells with the AhR agonist, 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD), and demonstrated that AhR activation increased the expression of both cytochrome P450 s and inflammatory markers. We also found increased mucin 5AC production with TCDD treatment. Similar results were observed in NCI-H441 cells treated with urban dust particles. Mucin 5AC expression was highly correlated with increased-expression cyclooxygenase-2 and IL-1beta, thus implicating these two inflammatory markers as possible conduits for AhR-mediated mucin production. We hypothesize that this increase in mucin 5AC production is a result of inflammation-induced differentiation of our epithelial cell to a mucin-producing cell. This theory is supported by morphological changes observed in the cells, as well as decreased expression of Clara cell secretory protein (CC10). In an in vivo C57BL/6 mouse model, TCDD increased expression of inflammatory cytokines, mucin 5AC, and a number of matrix metalloproteases in whole-lung samples. These changes were not seen in mice in which AhR signaling was repressed. These markers from the whole-lung samples have been correlated to onset of bronchitis, asthma, small airways disease, and fibrosis, and their increased expression further implicates AhR activation in producing the molecular environment for the development of lung injury to occur.
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PMID:Arylhydrocarbon receptor activation in NCI-H441 cells and C57BL/6 mice: possible mechanisms for lung dysfunction. 1937 48


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